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Diagnostic sensitivity of high-sensitivity troponin T in acute myocardial infarction in patients with chest pain
Milan Hromádka, Dan Rajdl, Ladislav Trefil, Jaroslav Racek, Richard Rokyta
Jazyk angličtina Země Česko
- Klíčová slova
- vysoce senzitivní troponin T, diagnostická citlivost, bolest na hrudi, akutní infarkt myokardu,
- MeSH
- akutní nemoc MeSH
- bolesti na hrudi diagnóza etiologie MeSH
- elektrokardiografie využití MeSH
- financování organizované MeSH
- hospitalizace statistika a číselné údaje MeSH
- infarkt myokardu diagnóza epidemiologie krev MeSH
- lidé MeSH
- senzitivita a specificita MeSH
- troponin I MeSH
- troponin T diagnostické užití MeSH
- Check Tag
- lidé MeSH
Introduction: The diagnosis of acute myocardial infarction (AMI) is based on an increase in plasma troponin levels above the 99th percentile of a healthy reference population values. On admission, over 30% of patients with AMI do not have specific symptoms and up to 70% of them may have normal or non-diagnostic ECG recordings. In these patient subgroups cardiac troponin assays may play a critical role in diagnosing AMI. Several diagnostic kits with enhanced analytic sensitivity (high-sensitivity kits) have been developed recently. Aim of study: To compare diagnostic sensitivity of troponin I (cTnI) and high-sensitivity troponin T (hs-cTnT) in the diagnosis of acute myocardial infarction in patients with chest pain. Type of study: Prospective, observational. Patients and methods: We evaluated prospectively 107 consecutive patients [median (interquartile range) age: 64 (55–75) years; 29 women] admitted to intensive cardiac care unit for chest pain, with admission cTnI levels o0.1 mg/l. In all patients, the parameters determined on admission included their levels of cTnI (chemiluminiscence immunoassay with microparticles, Abbott, Architect i2000 analyzer), hs-cTnT (electrochemiluminiscence immunoassay; Roche Cobas e411 analyzer), and myoglobin (immunoturbidimetry). The diagnosis of AMI was established by the attending cardiologist (using the ‘‘universal’’ definition of acute myocardial infarction). The cTnI and hs-cTnT cut-off values for AMI were 0.033 mg/l and 14 ng/l, respectively. Troponin I levels were again determined at 6 and 12 h after admission. Results: A total of 50 patients (46.7%) were diagnosed to have AMI with ST-segment elevation (STEMI), 35 patients (32.7%) developed AMI without STE (non-STEMI), 10 patients (9.3%) experienced a Type 2 AMI, four patients (3.7%) had unstable angina, and eight patients (7.5%) chest pain of non-coronary etiology (most often vertebrogenic pain). The diagnostic sensitivity of admission cTnI and hs-cTnT levels for AMI was 72% and 78%, respectively (p¼0.1814). The correlation between cTnI and hs-cTnT was 0.67 (po0.001; Spearman rank correlation coefficient). The diagnostic sensitivity of admission hs-cTnT and cTnI in STEMI patients was 82% vs. 70%, respectively (p¼0.0771). In non-STEMI patients, similar baseline cTnI and hs-cTnT diagnostic sensitivity was found, 74.3% and 71.4%, respectively (p¼0.91).
Kardiologické oddělení Komplexní kardiovaskulární centrum UK Praha LF a FN Plzeň
Ústav klinické biochemie a hematologie UK Praha LF a FN Plzeň
Obsahuje 3 tabulky
Bibliografie atd.Literatura
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- $a Introduction: The diagnosis of acute myocardial infarction (AMI) is based on an increase in plasma troponin levels above the 99th percentile of a healthy reference population values. On admission, over 30% of patients with AMI do not have specific symptoms and up to 70% of them may have normal or non-diagnostic ECG recordings. In these patient subgroups cardiac troponin assays may play a critical role in diagnosing AMI. Several diagnostic kits with enhanced analytic sensitivity (high-sensitivity kits) have been developed recently. Aim of study: To compare diagnostic sensitivity of troponin I (cTnI) and high-sensitivity troponin T (hs-cTnT) in the diagnosis of acute myocardial infarction in patients with chest pain. Type of study: Prospective, observational. Patients and methods: We evaluated prospectively 107 consecutive patients [median (interquartile range) age: 64 (55–75) years; 29 women] admitted to intensive cardiac care unit for chest pain, with admission cTnI levels o0.1 mg/l. In all patients, the parameters determined on admission included their levels of cTnI (chemiluminiscence immunoassay with microparticles, Abbott, Architect i2000 analyzer), hs-cTnT (electrochemiluminiscence immunoassay; Roche Cobas e411 analyzer), and myoglobin (immunoturbidimetry). The diagnosis of AMI was established by the attending cardiologist (using the ‘‘universal’’ definition of acute myocardial infarction). The cTnI and hs-cTnT cut-off values for AMI were 0.033 mg/l and 14 ng/l, respectively. Troponin I levels were again determined at 6 and 12 h after admission. Results: A total of 50 patients (46.7%) were diagnosed to have AMI with ST-segment elevation (STEMI), 35 patients (32.7%) developed AMI without STE (non-STEMI), 10 patients (9.3%) experienced a Type 2 AMI, four patients (3.7%) had unstable angina, and eight patients (7.5%) chest pain of non-coronary etiology (most often vertebrogenic pain). The diagnostic sensitivity of admission cTnI and hs-cTnT levels for AMI was 72% and 78%, respectively (p¼0.1814). The correlation between cTnI and hs-cTnT was 0.67 (po0.001; Spearman rank correlation coefficient). The diagnostic sensitivity of admission hs-cTnT and cTnI in STEMI patients was 82% vs. 70%, respectively (p¼0.0771). In non-STEMI patients, similar baseline cTnI and hs-cTnT diagnostic sensitivity was found, 74.3% and 71.4%, respectively (p¼0.91).
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